Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology

摘要: Ischaemic postconditioning (brief periods of ischaemia alternating with brief reflow applied at the onset reperfusion following sustained ischaemia) effectively reduces myocardial infarct size in all species tested so far, including humans. is a simple and safe manoeuvre, but because injury initiated within minutes reflow, must be reperfusion. The mechanisms protection by include: formation release several autacoids cytokines; maintained acidosis during early reperfusion; activation protein kinases; preservation mitochondrial function, most strikingly attenuation opening permeability transition pore (MPTP). Exogenous recruitment some identified signalling steps can induce cardioprotection when time animal experiments, more recently was also observed proof-of-concept clinical trial. Indeed, studies patients an acute infarction showed reduction improved left ventricular function they underwent ischaemic or pharmacological inhibition MPTP interventional Further large-scale human are needed to determine whether different co-morbidities co-medications respond equally postconditioning. Also, our understanding underlying develop new therapeutic strategies ultimate aim limiting burden heart disease potentially providing for other organs risk injury, such as brain kidney.